Pascale Texier

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This study describes the physical and functional interactions between ICP0 of herpes simplex virus type 1 and class II histone deacetylases (HDACs) 4, 5, and 7. Class II HDACs are mainly known for their participation in the control of cell differentiation through the regulation of the activity of the transcription factor MEF2 (myocyte enhancer factor 2),(More)
Spinal muscular atrophy (SMA) is a muscular disease characterized by the death of motoneurons, and is a major genetic cause of infant mortality. Mutations in the SMN1 gene, which encodes the protein survival motor neuron (SMN), are responsible for the disease. SMN belongs to the Tudor domain protein family, whose members are known to interact with(More)
Interphase centromeres are crucial domains for the proper assembly of kinetochores at the onset of mitosis. However, it is not known whether the centromere structure is under tight control during interphase. This study uses the peculiar property of the infected cell protein 0 of herpes simplex virus type 1 to induce centromeric structural damage, revealing(More)
During herpes simplex virus type 1 (HSV-1) latent infection in vivo, the latency-associated promoter (LAP) is the only promoter to remain highly active long term. In a previous attempt to characterize LAP activity in vitro and in a mouse model, we showed that a 1.5-kb fragment called the long-term expression element (LTE), located immediately downstream(More)
This study describes the nucleolar localization of the viral protein ICP0 of herpes simplex virus type 1. We show that the RING finger domain of ICP0 is essential for ICP0 to localize in nucleoli of transfected and 4 hour-infected cells. ICP0 forms particular intranucleolar domains that do not correspond to any known nucleolar domains. This distribution was(More)
Herpes simplex virus 1 (HSV-1) establishes latency in trigeminal ganglia (TG) sensory neurons of infected individuals. The commitment of infected neurons toward the viral lytic or latent transcriptional program is likely to depend on both viral and cellular factors, and to differ among individual neurons. In this study, we used a mouse model of HSV-1(More)
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